In fat grafting, macrophages and their polarization initiated changes in the levels of dominant secreted factors and influenced blood-derived stem cell infiltration, indicating that macrophages were crucial for tissue revascularization. The macrophage manipulation models described here show that graft macrophage number can profoundly influence graft survival.

Stromal vascular fraction gel has a high long-term retention rate and a unique adipose regeneration mode, involving prompt inflammation and infiltration of immune cells, stimulating rapid angiogenesis and inducing host cell-mediated adipogenesis.

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BackgroundHypertrophic scars cause cosmetic and functional problems for patients, and their treatment remains challenging. Mechanical micronization of adipose tissue can remove adipocytes and concentrate functional cells. Stromal vascular fraction (SVF)-gel is obtained by a series of simple mechanical processes, including shifting between syringes and centrifugation. This study aimed to assess the therapeutic effect of SVF-gel on hypertrophic scars.MethodsA model of hypertrophic scars was established in rabbit ears. SVF-gel and SVF cells were obtained from rabbit inguinal fat pads and injected into scars. Phosphate-buffered saline (PBS) was used as a control. Scars were structurally characterized by histologic and immunohistochemical analyses. Expression of inflammatory and fibrogenic genes was evaluated.ResultsHypertrophic scars became less visible and softer following injection of SVF-gel or SVF cells. Dermal thickness was significantly lower in the groups treated with SVF-gel and SVF cells than in the PBS-treated group. Treatment with SVF-gel restored subcutaneous fat tissue in scars, while treatment with SVF cells and PBS did not. Injection of SVF-gel and SVF cells reduced macrophage infiltration in the dermal layer and decreased mRNA expression of interleukin-6 and monocyte chemoattractant protein-1. In addition, the level of myofibroblasts and collagen deposition were reduced in the groups treated with SVF-gel and SVF cells.ConclusionsSVF-gel has therapeutic effects on hypertrophic scars. Injection of SVF-gel into hypertrophic scars restores subcutaneous fat tissue and reduces the levels of macrophages and myofibroblasts; thus, it decreased the dermal thickness of the scar.

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Background: Fat grafting is a popular soft-tissue filler method; however, the mechanism of its survival and regeneration is still not fully understood. Neutrophils are the frontier inflammatory cells and closely associated with tissue regeneration. To understand the role of neutrophils in fat graft retention, we adopted neutrophil depletion and up-regulation models. Methods: Mouse inguinal fat (approximately 200 mg) was transferred autologously. The anti-mouse Ly6G antibody and lipopolysaccharides were used in the mouse fat grafting model for neutrophil depletion or activation, respectively. We examined the blood and graft stromal vascular fraction by fluorescence-activated cell sorting in manipulation/control groups. Graft weight, vascularization, and secreted factors were also compared. Results: There was a significant reduction/increase of neutrophil counts in the circulation and the transferred fat before day 7 with Ly6G antibody/lipopolysaccharides treatment. Early depletion of neutrophils resulted in incompetent angiogenesis and eventually a poor retention rate (27 ± 8 percent) compared with control (51 ± 10 percent; p < 0.05), whereas up-regulated neutrophils increased the inflammation and reactive oxygen species level, leading to tissue damage and poor retention rate (20 ± 9 percent) compared with control (51 ± 10 percent; p < 0.05). Enhanced macrophage infiltration could be found in both neutrophil depletion and up-regulation groups after week 4. Conclusions: Undisturbed neutrophil function is the key to initiating downstream responses of macrophage infiltration, stimulating vessel formation, and regulating inflammation level; thus, it exerts a great impact on the long-term retention rate. Disturbed neutrophil function, either enhanced or weakened, can lead to impaired fat graft retention.

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